Please use this identifier to cite or link to this item: https://doi.org/10.1007/s12253-011-9485-5
Title: RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status
Authors: Omar, M.F.M.
Ito, K.
Nga, M.E.
Soo, R. 
Peh, B.K. 
Ismail, T.M.
Thakkar, B. 
Soong, R. 
Ito, Y.
Salto-Tellez, M. 
Keywords: EGFR
KRAS
Lung adenocarcinoma
P53
Promoter hypermethylation
RUNX3
Issue Date: Oct-2012
Source: Omar, M.F.M., Ito, K., Nga, M.E., Soo, R., Peh, B.K., Ismail, T.M., Thakkar, B., Soong, R., Ito, Y., Salto-Tellez, M. (2012-10). RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status. Pathology and Oncology Research 18 (4) : 783-792. ScholarBank@NUS Repository. https://doi.org/10.1007/s12253-011-9485-5
Abstract: RUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMAwas also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications. © Arányi Lajos Foundation 2012.
Source Title: Pathology and Oncology Research
URI: http://scholarbank.nus.edu.sg/handle/10635/116580
ISSN: 12194956
DOI: 10.1007/s12253-011-9485-5
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